Respiratory Muscle Function and Hypoxia: Role of Nitric Oxide.
Year: 2006
Type: article
Abstract: Hypoxia disturbs the Ca regulation and increases the intracellular Ca concentration ([Ca]i), which may in turn activate nitric oxide (NO) synthase regulated by [Ca]i. Since NO reduces the isometric contractility of rat diaphragm in vitro, we hypothesize that NO contributes to impaired force generation of hypoxic diaphragm. The effects of different concentrations of the NOS inhibitor, NMonomethyl-L-arginine (L-NMMA), the NO scavenger hemoglobin (150 μM) and the NO donor Spermine NONOate (Sp-NO; 1 mM) were determined on isometric contractility during hypoxia (Po2 ~ 7 kPa (~ 54 mmHg)) and hyperoxia (Po2 ~ 83 kPa (~ 639 mmHg)). Hypoxia significantly reduced maximal twitch tension (Pt), and submaximal tetanic tension (30 Hz, P30) in all L-NMMA groups. Low concentration of L-NMMA (30 μM) increased P30 but high concentration of L-NMMA (1000 μM) reduced P30 during hypoxia. The effects of L-NMMA on force generation were more pronounced during hypoxia compared to hyperoxia. Peak increases in P30 and Pt were observed with a concentration of 30 μM L-NMMA during hypoxia, but with 10 μM L-NMMA during hyperoxia. The same concentration of hemoglobin increased P30 and Pt less during hypoxia compared to hyperoxia. Sp-NO reduced Pt, P30 and maximal tetanic tension (Po) during hypoxia; these effects were abolished in the presence of hemoglobin. Sp-NO did not alter Pt, P30 and Po during hyperoxia. We conclude that NO plays a more prominent role during hypoxia and that NO contributes to the depression of force generation of hypoxic rat diaphragm in vitro. This change may be related to elevated NO generation within the hypoxic diaphragm.
Author: Xiaoping Zhu
Language: English
Subfield: Physiology (medical)
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W1483523718